GWAS, Cytomegalovirus Infection, and Schizophrenia

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  • Jakob Grove
  • Anders Børglum
  • Brad D Pearce, Center for Translational Social Neuroscience, Emory University, Atlanta, GA, USA, Department of Epidemiology (RSPH), Emory University, Office: 1518 Clifton Rd. CNR 4049 (1518-002-AA), Atlanta, GA, 30322, USA, United States
In recent years, good progress has been made in uncovering the genetic underpinnings of schizophrenia. Even so, as a polygenic disorder, schizophrenia has a complex etiology that is far from understood. Meanwhile, data are being collected enabling the study of interactions between genes and the environment. A confluence of data from genetic and environmental exposure studies point to the role of infections and immunity in the pathophysiology of schizophrenia. In a recent study by Børglum et al., a single nucleotide polymorphism (SNP) in the gene CTNNA3 was identified that may provide clues to gene-environment interactions. The carriers of the minor allele for the SNP had a fivefold risk of later developing schizophrenia if their mothers were CMV positive, while the children not carrying the allele had no excess risk from maternal CMV. In the current paper, we summarize recent advances to clarify a possible mechanism of such interactions between the host genotype and infection in schizophrenia risk.
Original languageEnglish
JournalCurrent Behavioral Neuroscience Reports
Pages (from-to)215-223
Publication statusPublished - Dec 2014

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